OBJECTIVES: To explore the efficacy of DSA-guided intrathecal drug delivery system combined with Zi Wu Liu Zhu Acupoint Therapy for management of cancer pain and provide reference for its standardized clinical application. Methods and. RESULTS: Recommendations were formulated based on literature review and expert group discussion, and consensus was reached following expert consultation. The consensus recommendations are comprehensive, covering the entire treatment procedures from preoperative assessment and preparation, surgical operation process, postoperative management and traditional Chinese medicine treatment to individualized treatment planning. The study results showed that the treatment plans combining traditional Chinese with Western medicine effectively alleviated cancer pain, reduced the use of opioid drugs, and significantly improved the quality of life and enhanced immune function of the patients. Postoperative follow-up suggested good treatment tolerance among the patients without serious complications. CONCLUSIONS The formulated consensus is comprehensive and can provide reference for clinicians to use DSA-guided intrathecal drug delivery system combined with Zi Wu Liu Zhu Acupoint Therapy. The combined treatment has a high clinical value with a good safety profile for management of cancer pain.
Humans ; Medicine, Chinese Traditional ; Cancer Pain/therapy* ; Drugs, Chinese Herbal/therapeutic use* ; Drug Delivery Systems ; Pain Management/methods* ; China

Objective:To investigate the safety and effectiveness of multi-stent overlapping assisted coil embolization for ruptured intracranial blood blister-like aneurysms (BBA).Methods:Patients with intracranial BBA admitted to the Affiliated Quanzhou First Hospital of Fujian Medical University and treated with multi-stent overlapping assisted coil embolization from January 2013 to January 2019 were enrolled retrospectively. The embolization rate immediately after procedure, modified Rankin Scale (mRS) score at discharge, aneurysm embolization rate, recurrence rate and mRS scores at 3 months after procedure were collected.Results:A total of 38 patients with BBA were enrolled, including 21 females (55.3%) and 17 males (44.7%); their age was 54±9.3 years (range, 29-71 years); the maximum diameter of aneurysm was 5.1±1.0 mm, and the diameter of aneurysm neck was 4.9±0.7 mm. Raymond grading showed that the complete embolization rate immediate after procedure was 71.1%, the residual rate of aneurysmal neck was 18.4%, and the residual rate of aneurysmal body was 10.5%. During the perioperative period, 2 patients had stent thrombosis and 2 had intraoperative aneurysm hemorrhage. Imaging follow-up at 3 months after procedure showed that the aneurysms of 31 cases (83.8%) disappeared completely, 4 (10.8%) improved, and 2 (5.4%) recanalized. The good clinical outcome rate (mRS score ≤ 2) was 81.1%, 1 patient (2.6%) died, and no postoperative rebleeding occurred.Conclusion:Multi-stent overlapping assisted coil embolization is a safe and effective surgical method for the treatment of ruptured intracranial BBA.

Objective:To investigate the pathological characteristics and the clinical significance of novel coronavirus (2019-nCoV)-infected pneumonia (termed by WHO as coronavirus disease 2019, COVID-19).Methods:Minimally invasive autopsies from lung, heart, kidney, spleen, bone marrow, liver, pancreas, stomach, intestine, thyroid and skin were performed on three patients died of novel coronavirus pneumonia in Chongqing, China. Hematoxylin and eosin staining (HE), transmission electron microcopy, and histochemical staining were performed to investigate the pathological changes of indicated organs or tissues. Immunohistochemical staining was conducted to evaluate the infiltration of immune cells as well as the expression of 2019-nCoV proteins. Real time PCR was carried out to detect the RNA of 2019-nCoV.Results:Various damages were observed in the alveolar structure, with minor serous exudation and fibrin exudation. Hyaline membrane formation was observed in some alveoli. The infiltrated immune cells in alveoli were majorly macrophages and monocytes. Moderate multinucleated giant cells, minimal lymphocytes, eosinophils and neutrophils were also observed. Most of infiltrated lymphocytes were CD4-positive T cells. Significant proliferation of type Ⅱ alveolar epithelia and focal desquamation of alveolar epithelia were also indicated. The blood vessels of alveolar septum were congested, edematous and widened, with modest infiltration of monocytes and lymphocytes. Hyaline thrombi were found in a minority of microvessels. Focal hemorrhage in lung tissue, organization of exudates in some alveolar cavities, and pulmonary interstitial fibrosis were observed. Part of the bronchial epithelia were exfoliated. Coronavirus particles in bronchial mucosal epithelia and type Ⅱ alveolar epithelia were observed under electron microscope. Immunohistochemical staining showed that part of the alveolar epithelia and macrophages were positive for 2019-nCoV antigen. Real time PCR analyses identified positive signals for 2019-nCoV nucleic acid. Decreased numbers of lymphocyte, cell degeneration and necrosis were observed in spleen. Furthermore, degeneration and necrosis of parenchymal cells, formation of hyaline thrombus in small vessels, and pathological changes of chronic diseases were observed in other organs and tissues, while no evidence of coronavirus infection was observed in these organs.Conclusions:The lungs from novel coronavirus pneumonia patients manifest significant pathological lesions, including the alveolar exudative inflammation and interstitial inflammation, alveolar epithelium proliferation and hyaline membrane formation. While the 2019-nCoV is mainly distributed in lung, the infection also involves in the damages of heart, vessels, liver, kidney and other organs. Further studies are warranted to investigate the mechanism underlying pathological changes of this disease.

Objective To investigate the expressions of Krüppel like factor 5 (KLF5) and tumor necrosis factor receptor superfamily member 11a (TNFRSF11a) in cervical cancer tissues and their effect on proliferation,migration,and invasion of HeLa cells. Methods Microarray technology was used to detect the mRNA expression of gene in cytocine stimulusin cervical tissues,and the result was verified by real-time fluorescence quantitative polymerase chain reaction. The expressions of KLF5 and TNFRSF11a in cervical tissues were detected by double immunofluorescence staining. HeLa cells were transfected with specific small interfering RNA to knock down the endogenous TNFRSF11a and KLF5 and were infected with adenovirus containing KLF5 to over-express KLF5,respectively. Protein level was detected by Western blot. The regulatory effect of KLF5 on candidate target gene (TNFRSF11a) was determined by dual-luciferase reporter assay. The activity of the cell proliferation,migration,and invasion was detected by using cell counting kit-8 assay and Transwell assay. Results The results of microarray technology showed that the expressions of KLF5 and TNFRSF11a were significantly higher in cervical squamous cell carcinoma tissues compared with normal cervical tissues (P=0.002,P=0.045),and real-time fluorescence quantitative polymerase chain reaction showed that the mRNA expressions of KLF5 and TNFRSF11a were significantly higher in cervical intraepithelial neoplasia (CIN) Ⅰ,CINⅡ-Ⅲ and cervical squamous cell carcinoma tissues compared with normal cervical tissues (KLF5:F=32.79,P=0.018,P=0.014,and P=0.011;TNFRSF11a:F=36.72,P=0.013,P=0.010,and P=0.009) and double immunofluorescence staining showed that the protein expressions of KLF5 and TNFRSF11a were significantly higher in CIN Ⅰ,CIN Ⅱ-Ⅲ and cervical squamous cell carcinoma tissues compared with normal cervical tissues (KLF5:F=42.38,P=0.014,P=0.008,and P=0.002;TNFRSF11a:F=35.42,P=0.021,P=0.012,and P=0.004) and increased with the carcinogenesis. The experiment in vitro confirmed that KLF5 promotes proliferation,migration,and invasion of HeLa by up-regulating TNFRSF11a expression. Clinical analysis showed that the expression of TNFRSF11a mRNA was positively correlated with tumor pathological grading,clinical stage,depth of invasion,and lymph node metastasis (all P<0.05). Conclusion KLF5 and TNFRSF11a are related to cervical cancer. KLF5 promote the proliferation,migration,and invasion of cervical cancer cells partly by upregulating the transcription of TNFRSF11a.

[Objective] To summarize the experience of professor FAN Yongsheng who uses the herbal prescription"modified Simiao powder"to treat gouty arthritis, so as to direct our clinical practice better. [Method] By learning from professor FAN as well as collating his medical cases that applicating "modified Simiao powder" to the treatment of gouty arthritis, clearing and definiting how teacher FAN thinks etiologies and pathogenesis of gouty arthritis and analyzing the prescription of"Simiao powder"and giving two clinical cases, so that we can learn and discuss. [Result] Teacher FAN believes that gout pathogenesis for the body fluid metabolic abnormalities, and body fluid metabolism and liver and spleen and kidney three organs are closely related. Patients usually irritable or liver qi stagnation, or like to eat greasy meat, temper deficiency, or lack of kidney essence, gasification weakness, resulting in wet endogenous, wet evil staying in the joints, the emergence of local fever, phlegm, blood stasis, poisonous evil, into gouty arthritis. Acute onset of the pathogenesis of "hot and humid", the course of time for the "hot and humid phlegm stagnant each other", treatment should follow the law of "clear away heat-dampness", according to the cause, changes in the pathogenesis of flexible application of four wonderful addition and subtraction; And to Qufeng, detoxification, blood circulation, dredge meridian, so as to achieve dialectical treatment, with the card addition and subtraction. [Conclusion] Professor FAN Yongsheng uses"modified Simiao powder"to treat gouty arthritis and has achieved good clinical efficacy, worthy of clinical study and reference.

Objective To explore the molecular mechanisms of resistance to phosphatidyl inositol 3?kinase ( PI3K) inhibitors in triple?negative breast cancer ( TNBC) cells. Methods HCC70 cells ( TNBC) were transfected with siFZD7, siWANT5B or siGSK3 using lipofectamine 2000 transfection reagent. The expression levels of key proteins of WNT/β?catenin and PI3K/AKT/mTOR pathways were determined by Western blot analysis. After HCC70, MCF?7 ( ER?positive ) and SK?BR3 ( HER2?positive ) cells were treated with PI3K/AKT/mTOR inhibitors, the inhibition rates of cell proliferation were measured by MTT assay, and half maximal inhibitory concentrations ( IC50 ) were calculated. The altered activities of WNT/β?catenin and PI3K/AKT/mTOR proteins were detected by Western blot and luciferase report gene assay, respectively. The nuclear translocation of β?catenin protein was examined by immunofluorescence assay. Xenograft nude mouse model was used to evaluate the tumorigenicity of breast cancer cells treated with BKM120 in vivo. The expression levels of p?LRP6, p?4EBP1 and β?catenin proteins in the tumor tissues were determined by immunohistochemical staining. Results The expression levels of FZD7, WANT5B and GSK3 proteins were significantly reduced in the HCC70 cells transfected with the target siRNAs. Meanwhile, the activity of WNT/β?catenin was enhanced and PI3K/AKT/mTOR pathway was inhibited. PI3K/AKT/mTOR inhibitors suppressed MCF?7 and SK?BR3 cell proliferation. The IC50 of GDC?094, BKM120, XL147, perifosine, everolimus, and BEZ235 in MCF?7 cells were 0. 46 mmol/L, 1. 44 mmol/L, 4. 34 mmol/L, 11.35 μmol/L, 53. 71 μmol/L and 12. 87 μmol/L respectively, and 0. 63 mmol/L, 0. 58 mmol/L, 3. 74 mmol/L, 13.22μmol/L, 60.00μmol/L and 11.38μmol/L in the SK?BR3 cells, respectively. The results of luciferase report gene assay showed that the luciferase activities in HCC70, MCF?7 and SK?BR3 cells treated with BKM120 were 1.75±0.05, 1.13±0.02 and 0.43±0.01, respectively. The luciferase activities in HCC70 and SK?BR3 cells were significantly different from that of the control cells (1.00±0.02, P<0.05). The immunohistochemical analysis showed that BKM120 inhibited mTOR activity, and the enhanced WNT/β?catenin activity reversed the phenotype of inhibitory mTOR induced by BKM120. BKM120 suppressed the tumorigenic ability of MCF?7 and SK?BR3 cells in vivo, but had no effect on cultured HCC70 cells. The immunohistochemical analysis showed nuclear translocation of β?catenin protein and increased expression level of p?LRP?6 protein in transplanted tumor tissues from HCC70 cells treated with BKM120, increased the level of p?LRP?6 protein, and no changes of p?4EBP1 protein expression. However, no nuclear translocation of β?catenin protein and no decrease of p?LRP6 and p?4EBP1 protein levels in the transplanted tumor tissue of MCF?7 cells after treatment with BKM120. Conclusions The triple?negative breast cancer HCC70 cells have drugs?resistance to PI3K inhibitors. The WNT/β?catenin signaling pathway may regulate the PI3K/AKT/mTOR pathway, therefore, inducing the drug?resistance of TNBC cells to PI3K inhibitors.

Objective To explore the molecular mechanisms of resistance to phosphatidyl inositol 3?kinase ( PI3K) inhibitors in triple?negative breast cancer ( TNBC) cells. Methods HCC70 cells ( TNBC) were transfected with siFZD7, siWANT5B or siGSK3 using lipofectamine 2000 transfection reagent. The expression levels of key proteins of WNT/β?catenin and PI3K/AKT/mTOR pathways were determined by Western blot analysis. After HCC70, MCF?7 ( ER?positive ) and SK?BR3 ( HER2?positive ) cells were treated with PI3K/AKT/mTOR inhibitors, the inhibition rates of cell proliferation were measured by MTT assay, and half maximal inhibitory concentrations ( IC50 ) were calculated. The altered activities of WNT/β?catenin and PI3K/AKT/mTOR proteins were detected by Western blot and luciferase report gene assay, respectively. The nuclear translocation of β?catenin protein was examined by immunofluorescence assay. Xenograft nude mouse model was used to evaluate the tumorigenicity of breast cancer cells treated with BKM120 in vivo. The expression levels of p?LRP6, p?4EBP1 and β?catenin proteins in the tumor tissues were determined by immunohistochemical staining. Results The expression levels of FZD7, WANT5B and GSK3 proteins were significantly reduced in the HCC70 cells transfected with the target siRNAs. Meanwhile, the activity of WNT/β?catenin was enhanced and PI3K/AKT/mTOR pathway was inhibited. PI3K/AKT/mTOR inhibitors suppressed MCF?7 and SK?BR3 cell proliferation. The IC50 of GDC?094, BKM120, XL147, perifosine, everolimus, and BEZ235 in MCF?7 cells were 0. 46 mmol/L, 1. 44 mmol/L, 4. 34 mmol/L, 11.35 μmol/L, 53. 71 μmol/L and 12. 87 μmol/L respectively, and 0. 63 mmol/L, 0. 58 mmol/L, 3. 74 mmol/L, 13.22μmol/L, 60.00μmol/L and 11.38μmol/L in the SK?BR3 cells, respectively. The results of luciferase report gene assay showed that the luciferase activities in HCC70, MCF?7 and SK?BR3 cells treated with BKM120 were 1.75±0.05, 1.13±0.02 and 0.43±0.01, respectively. The luciferase activities in HCC70 and SK?BR3 cells were significantly different from that of the control cells (1.00±0.02, P<0.05). The immunohistochemical analysis showed that BKM120 inhibited mTOR activity, and the enhanced WNT/β?catenin activity reversed the phenotype of inhibitory mTOR induced by BKM120. BKM120 suppressed the tumorigenic ability of MCF?7 and SK?BR3 cells in vivo, but had no effect on cultured HCC70 cells. The immunohistochemical analysis showed nuclear translocation of β?catenin protein and increased expression level of p?LRP?6 protein in transplanted tumor tissues from HCC70 cells treated with BKM120, increased the level of p?LRP?6 protein, and no changes of p?4EBP1 protein expression. However, no nuclear translocation of β?catenin protein and no decrease of p?LRP6 and p?4EBP1 protein levels in the transplanted tumor tissue of MCF?7 cells after treatment with BKM120. Conclusions The triple?negative breast cancer HCC70 cells have drugs?resistance to PI3K inhibitors. The WNT/β?catenin signaling pathway may regulate the PI3K/AKT/mTOR pathway, therefore, inducing the drug?resistance of TNBC cells to PI3K inhibitors.

ObjectiveTo review the experience of video-assisted thoracoscopic resection for posterior mediastinal neurogenic tumors,to investigate the technical features and difficulties of thoracoscopic approach.MethodsFrom May 2001 to June 2011,58 patients underwent thoracoscopic resection of posterior mediastinal tumors in our institution,including 36 males and 22 females.The average age of the patients was 38.7 years.The average tumor size was 4.9 cm.16 patients had neurogenic or pulmonary symptoms at the time of diagnosis,while the other 42 were asymptomic.24 lesions were located in the left side,33 lesions in the right side,1 lesion in bilateral sides.All procedures generally required 3 ports,and intracapsular enucleation was preferred,supplying vessels were ligated by hemoclips or Hem-o-lock clips; the nerves of origin were cut off at both edges of the tumor.For bulky tumor,dense adhesion,and massive bleeding,open conversions were performed by extending the incision anteriorly to 6-10 cm.ResultsAll procedures were successfully performed without death event occurring.The average operating time was 127.2 min.The average intraoperative blood loss was 206.4 ml.3 cases requied blood transfusion.The average chest tube duration was 2.72 days.The average postoperative stay was 5.19 days.53 procedures were performed entirely under thoracoscopy to achieve gross-total resection.Conversions to an open procedure were necessitated in 5 patients (8.6％).7 patients experienced post-operative complications,with 4 Horner syndromes.There were 25 neurilemomas,23 neurofibromas,8 ganglioneuromas,1 paraganglioma,and 1 malignant paraganglioma.No local recurrence was seen after an average follow-up of 44.9 months.ConclusionVideo-assisted thoracoscopic removes of the posterior mediastinal tumors are safe,reliable and minimally invasive for selected patients with mastered throcoscopic skills.intracapsular enucleation is a safe procedure with reduced risk,while tumors larger than 6cm and located in the apex are with increased risk.

Objective To look for a standard way to cure uric acid calculi in transplanted kidney with medicine.Methods Under the guide of the standard and widespread metabolic evaluation, citrate and allopurinol were used to treat 4 patients with uric acid calculi after kidney transplantation. These two kinds of medicines were used in the long term together with other conservative treatment to prevent the recurrence of calculi.Results In these 4 cases, all clinical syndromes disappeared and all the calculi dissolved. After follow-up for 1～2 years, no recurrence of calculi was found. Conclusion Citrate should be used to dissolve uric acid calculi in transplanted kidney and to prevent the recurrence of calculi under the guide of the standard metabolic evaluation.